Statin use seems controversial on this forum and in the US in general. However, what many may not know is that the UK is in open war over statin use. Here is an article in yesterday's Daily Mail. The headline sets the tone:

"The deadly propaganda of the statin deniers: The drugs DO protect you from heart attacks but as this devastating investigation reveals thousands are refusing them"

The article targets three doctors that I follow, Dr. Zoe Harcombe PHD, Dr. Malcolm Kendrick MD. and Dr. Asheem Malhotra MD. The Daily Mail calls all three "deniers" and sprinkles the article liberally with the term "fake news". Here is Zoe Harcombe's initial response to the article.

From the Daily Mail piece:

"Last night Health Secretary Matt Hancock voiced his concern about the Ďpernicious liesí being circulated and added: ĎStatins play a huge role in keeping people at risk of cardiovascular disease healthy. Risking peopleís health by spreading reckless and ignorant misinformation claiming otherwise is completely unjustifiable.í"

From Dr. Harcombe's response:

"In the absence of access to the CTSU data, we must rely on the independent assessment of all evidence for the efficacy of statins presented in the form of numbers needed to treat (an absolute measure). This reports that, for primary prevention (the majority), for those taking statins for 5 years, no lives will be saved and between 2 and 15 times as many people will be harmed (muscle damage, type 2 diabetes) as helped (avoiding an event) (Ref 4)."

I am not sure who is winning the war or if the victor will have truth on their side. Your thoughts?

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"Oh, twice as much ain't twice as good
And can't sustain like one half could
It's wanting more that's gonna send me to my knees" - John Mayer

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Scour the data: there is simply no evidence statins work. (And they do measurable harm when patients develop Type 2. And there is ZERO evidence they do anything for older women.)

(Related: If any drug has an "iffy" reputation, ask your doctor about Number Needed to Treat. Insist on data and keep questioning until you're satisfied that the drug being recommended will likely do you more good than harm.)

Scour the data: there is simply no evidence statins work. (And they do measurable harm when patients develop Type 2. And there is ZERO evidence they do anything for older women.)

(Related: If any drug has an "iffy" reputation, ask your doctor about Number Needed to Treat. Insist on data and keep questioning until you're satisfied that the drug being recommended will likely do you more good than harm.)

Be careful. You will be labeled a denier and a purveyor of fake news. Cholesterol is an essential building block used by every cell. I am skeptical when I am told I need to lower it. I don't know that it is possible to capture all of the benefits/harms caused by altering such a pervasive bodily process. OTOH, there are a lot of metabolically sick folks. Maybe in a sick population it provides a net benefit.

__________________
"Oh, twice as much ain't twice as good
And can't sustain like one half could
It's wanting more that's gonna send me to my knees" - John Mayer

I am quite grateful that my cholesterol numbers are (just) below the warning threshold and that I show no signs of hear disease, so I haven't had to struggle with this question. If my physician suggested a statin, I would struggle with the decision.

I have read articles by some of those deniers and found their arguments pretty compelling. But I don’t know squat and there are far more knowledgeable professionals on the other side. Luckily my numbers are high but not by much so, in light of the potential side effects and the NNT, I don’t take them. My GP has no objection. DW, on the other hand, had much higher numbers and a bad family history so she was distraught when she developed statin related muscle problems. She is now on Repatha injections - a biweekly non-statin that blasts LDL down.

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Every man is, or hopes to be, an Idler. -- Samuel Johnson

Over 15 years ago I was taking the statin stuff for a short while. Tried all varieties. They were wonderfully effective in giving severe joint and muscle pains where I could barely walk 50 feet. Let alone practice JuJutsu. Gave me the case of the stupids, barely able to think or remember things. Having high numbers since age 20, and still do. Docs are still pushing the crap, at 71 I still and will always say NO. IMHO the stuff is a huge money maker for pharma and kickbacks to prescribers.

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There must be moderation in everything, including moderation.

OP thank you for this. DH just had 250 cholesterol blood check. His LDL is high. He refuses to take statins. His PCP is pushing very hard to take them. Could some of you post numbers? His reasons are many, side effects, is the science accurate? We're aware how studies can be swayed depending on who conducted them. This article by the NIH highlights false research study data.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182327/

OP thank you for this. DH just had 250 cholesterol blood check. His LDL is high. He refuses to take statins. His PCP is pushing very hard to take them. Could some of you post numbers? His reasons are many, side effects, is the science accurate? We're aware how studies can be swayed depending on who conducted them. This article by the NIH highlights false research study data.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182327/

OP thank you for this. DH just had 250 cholesterol blood check. His LDL is high. He refuses to take statins. His PCP is pushing very hard to take them. Could some of you post numbers? His reasons are many, side effects, is the science accurate? We're aware how studies can be swayed depending on who conducted them. This article by the NIH highlights false research study data.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182327/

Is his BMI in the normal range? If not he should try to reduce his weight first and exercise. There are alternatives to statins such as generic Cholestyramine and Colesevelam that are not systemic drugs that belong to a class of drugs called bile acid-binding resins. I know someone who had adverse reaction to several types of statins and his doctor put him on Cholestyramine with few side effects. Ask your husband to talk to his PCP about alternatives to statins. A small percentage of the population cannot tolerate statins and the drug can be outright dangerous to those people (muscle damage - rhabdomyolysis, kidney failure, and death). The person I know had adverse reactions to Lipitor and Baycol. Baycol was removed from the market after it was found to be responsible for a number of deaths in a short period of time.

Regardless of how high my cholesterol is it’s one thing I absolutely don’t worry about. I focus on healthy weight,etc. Harming a bunch of people to get one good outcome is ridiculous. I knew someone with a cholesterol level of 300 that lived to 90. I treat my HBP, asthma. It’s a solution to a problem that doesn’t exist and a huge money maker for drug companies.

If you have the time and the inclination and you love techy talk, here is a great overview of cholesterol and Dr. Peter Attia's views on it.

Note conclusion 22.

Here is one interesting quote that sums up the current state of chaos in the field of cholesterol and statins, IMHO:

Quote:

The body of literature implicating LDL as having a causal role, a necessary but not sufficient role in the pathogenesis of atherosclerosis is on a different level from the body of literature that gave us the food pyramid and the real challenge I think in this low carb community, this LDL-denying community, is they’re throwing the baby out with the bathwater. Now, part of that is because I think there are too many doctors who are too lazy at the other end of the spectrum. They just assume, “Well, statins or what we give everybody. You know, anybody who’s LDL-C is about 100 gets to be on a statin”, and these doctors are equally guilty in my mind of being ignorant and not thoughtful and not understanding the pathophysiology of the disease, but somewhere between these, is a measured space that requires a very careful consideration of the literature.

What comes through to me is that deciding who will most likely benefit from a statin and who won't is a very complicated process. It isn't easy.

Cholesterol is “just” another fancy organic molecule in our body but with an interesting distinction: we eat it, we make it, we store it, and we excrete it – all in different amounts.

The pool of cholesterol in our body is essential for life. No cholesterol = no life.

Cholesterol exists in 2 forms – unesterified or “free” (UC) and esterified (CE) – and the form determines if we can absorb it or not, or store it or not (among other things).

Much of the cholesterol we eat is in the form of CE. It is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason this occurs is that CE not only has to be de-esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route.

Re-absorption of the cholesterol we synthesize in our body (i.e., endogenous produced cholesterol) is the dominant source of the cholesterol in our body. That is, most of the cholesterol in our body was made by our body.

The process of regulating cholesterol is very complex and multifaceted with multiple layers of control. I’ve only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated.

Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up. To see an important reference on this topic, please look here.

Cholesterol and triglycerides are not soluble in plasma (i.e., they can’t dissolve in water) and are therefore said to be hydrophobic.

To be carried anywhere in our body, say from your liver to your coronary artery, they need to be carried by a special protein-wrapped transport vessel called a lipoprotein.

As these “ships” called lipoproteins leave the liver they undergo a process of maturation where they shed much of their triglyceride “cargo” in the form of free fatty acid, and doing so makes them smaller and richer in cholesterol.

Special proteins, apoproteins, play an important role in moving lipoproteins around the body and facilitating their interactions with other cells. The most important of these are the apoB class, residing on VLDL, IDL, and LDL particles, and the apoA-I class, residing for the most part on the HDL particles.

Cholesterol transport in plasma occurs in both directions, from the liver and small intestine towards the periphery and back to the liver and small intestine (the “gut”).

The major function of the apoB-containing particles is to traffic energy (triglycerides) to muscles and phospholipids to all cells. Their cholesterol is trafficked back to the liver. The apoA-I containing particles traffic cholesterol to steroidogenic tissues, adipocytes (a storage organ for cholesterol ester) and ultimately back to the liver, gut, or steroidogenic tissue.

All lipoproteins are part of the human lipid transportation system and work harmoniously together to efficiently traffic lipids. As you are probably starting to appreciate, the trafficking pattern is highly complex and the lipoproteins constantly exchange their core and surface lipids.

The measurement of cholesterol has undergone a dramatic evolution over the past 70 years with technology at the heart of the advance.

Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C. LDL-C is measured or most often estimated.

More advanced cholesterol measuring tests do exist to directly measure LDL-C (though none are standardized), along with the cholesterol content of other lipoproteins (e.g., VLDL, IDL) or lipoprotein subparticles.

The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile. NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug naÔve patients, before changes are noted in glucose or insulin levels.

The progression from a completely normal artery to a “clogged” or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues “fixing” the apoB containing particles in place AND making more space for more of them.

While inflammation plays a key role in this process, it’s the penetration of the endothelium and retention within the endothelium that drive the process.

The most common apoB containing lipoprotein in this process is certainly the LDL particle. However, Lp(a) and apoB containing lipoproteins play a role also, especially in the insulin resistant person.

If you want to stop atherosclerosis, you must lower the LDL particle number. Period.

At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal.

“A particle is a particle is a particle.” If you don’t know the number, you don’t know the risk.

With respect to laboratory medicine, two markers that have a high correlation with a given outcome are concordant – they equally predict the same outcome. However, when the two tests do not correlate with each other they are said to be discordant.

LDL-P (or apoB) is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study.

LDL-C is only a good predictor of adverse cardiac events when it is concordant with LDL-P; otherwise it is a poor predictor of risk.

There is no way of determining which individual patient may have discordant LDL-C and LDL-P without measuring both markers.

Discordance between LDL-C and LDL-P is even greater in populations with metabolic syndrome, including patients with diabetes. Given the ubiquity of these conditions in the U.S. population, and the special risk such patients carry for cardiovascular disease, it is difficult to justify use of LDL-C, HDL-C, and TG alone for risk stratification in all but the most select patients.

To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis (e.g., IMT) while holding LDL-P constant and then again holding LDL size constant. Only when you do this can you see that the relationship between size and event vanishes. The only thing that matters is the number of LDL particles – large, small, or mixed.

HDL-C and HDL-P are not measuring the same thing, just as LDL-C and LDL-P are not.

Secondary to the total HDL-P, all things equal it seems smaller HDL particles are more protective than large ones.

As HDL-C levels rise, most often it is driven by a disproportionate rise in HDL size, not HDL-P.

In the trials which were designed to prove that a drug that raised HDL-C would provide a reduction in cardiovascular events, no benefit occurred: estrogen studies (HERS, WHI), fibrate studies (FIELD, ACCORD), niacin studies, and CETP inhibition studies (dalcetrapib and torcetrapib). But, this says nothing of what happens when you raise HDL-P.

Don’t believe the hype: HDL is important, and more HDL particles are better than few. But, raising HDL-C with a drug isn’t going to fix the problem. Making this even more complex is that HDL functionality is likely as important, or even more important, than HDL-P, but no such tests exist to “measure” this.

Did you say “delay?”

That’s right. The question posed above did not ask how one could “prevent” or eliminate the risk cardiovascular disease, it asked how one could “delay” it. There is a difference. To appreciate this distinction, it’s worth reading this recent publication by Allan Sniderman and colleagues. Allan sent me a copy of this paper ahead of publication a few months ago in response to a question I had posed to him over lunch one day. I asked,

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The worst decisions are usually made in times of anger and impatience.

While I don’t take statins I would not place myself squarely in the drier camp. If my numbers were way higher or I had other CVD risk factors I would get a comprehensive lipid panel to see what’s going on and then consider whether statins are worth trying.

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Every man is, or hopes to be, an Idler. -- Samuel Johnson

This term "denier" is pejorative and seems meant to stifle dissent. I read the Sniderman article, and it seems fairly convincing that perhaps statins should be used earlier and then they might make a greater difference. But I wonder. Many people who escaped childhood infectious disease in the 19th century lived very long lives even by our modern criteria, and for the most part, it often seems that the increased years of life sometimes seen today do not give much if any increased health. Why was MI a rare diagnosis in prior centuries? It is not that there were not plenty of old people. Are we to think that the doctors were stupid? They managed to make many other diagnoses well enough. So I doubt this.

Ha

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"As a general rule, the more dangerous or inappropriate a conversation, the more interesting it is."-Scott Adams

A few years ago I was diagnosed with arteriosclerosis with a cardiac calcium score well over 1000. My cardiologist put me on a statin for the first time in my life, because my cholesterol numbers were not high prior to the diagnosis. My understanding is a statin does help prevent heart attacks in those patients with heart disease. I donít have any side effects that Iím aware of. My body tolerates the statin well, so Iím going to follow doctorís orders.

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